Phosphorylation of PTB1B at Ser50 by Akt impairs its ability to dephosphorylate the insulin receptor

Molecular Endocrinology

Volumn 15, Issue 10, 2001, Pages 1768-1780

  Ravichandran, L V ^a   Chen, H ^a   Li, Y ^a   Quon, M J ^a  

^a NATIONAL HEART LUNG AND BLOOD INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

INSULIN; INSULIN RECEPTOR; PROTEIN TYROSINE PHOSPHATASE; SERINE; AKT1 PROTEIN, HUMAN; ONCOPROTEIN; PHOSPHOSERINE; PROTEIN KINASE B; PROTEIN SERINE THREONINE KINASE; PROTEIN TYROSINE PHOSPHATASE 1B;

ANIMAL CELL; ARTICLE; AUTOPHOSPHORYLATION; DEPHOSPHORYLATION; ENZYME ACTIVITY; GENETIC TRANSFECTION; INSULIN SENSITIVITY; NONHUMAN; POSITIVE FEEDBACK; PRIORITY JOURNAL; PROTEIN PHOSPHORYLATION; SIGNAL TRANSDUCTION; AMINO ACID SEQUENCE; ANIMAL; CELL STRAIN 3T3; CELL STRAIN COS1; CHEMISTRY; CONSENSUS SEQUENCE; FEEDBACK SYSTEM; GENETICS; HUMAN; METABOLISM; MOLECULAR GENETICS; MOUSE; MUTATION; PHOSPHORYLATION; PLASMID;

3T3 CELLS; AMINO ACID SEQUENCE; ANIMALS; CONSENSUS SEQUENCE; COS CELLS; FEEDBACK; HUMANS; INSULIN; MICE; MOLECULAR SEQUENCE DATA; MUTATION; PHOSPHORYLATION; PHOSPHOSERINE; PLASMIDS; PROTEIN-SERINE-THREONINE KINASES; PROTEIN-TYROSINE-PHOSPHATASE; PROTO-ONCOGENE PROTEINS; PROTO-ONCOGENE PROTEINS C-AKT; RECEPTOR, INSULIN; SIGNAL TRANSDUCTION; TRANSFECTION;

EID: 85047682027     PISSN: 08888809     EISSN: None     Source Type: Journal    
DOI: 10.1210/mend.15.10.0711     Document Type: Article

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